GFAP and S100B are biomarkers of traumatic brain injury

Abstract

This study confirms that GFAP and S100B levels in serum are adjuncts to the assessment of brain damage after TBI and may enhance prognostication when combined with clinical variables.

GFAP-BDP as an Acute Diagnostic Marker in Traumatic Brain Injury: Results from the Prospective Transforming Research and Clinical Knowledge in Traumatic Brain Injury Study

“…In unfavorable compared to favorable outcome, GFAP was increased 20-fold and S100B was increased 2-fold. 20 Mean serum concentrations at hospital admission after SAH were increased (S100B threefold and GFAP twofold) compared with the upper limit of normal reference values. 21 Vos and colleagues reported that, in severe TBI patients, median serum levels of S100B, GFAP, and NSE were raised 18-fold (S100b), 5-fold (GFAP), and 2-fold (NSE), respectively, compared with normal reference values.…”

Brain inflammation induced by severe asphyxia in newborn pigs and the impact of alternative resuscitation strategies on the newborn central nervous system

“…The inflammatory protein S100 is identified as a good prognostic factor of neurological outcome after cardiac arrest and an early predictor of brain damage (11). S100 is a sensitive parameter for brain damage, and high levels of S100 in CSF and other biological fluids are associated with fatal outcome (12). Anticipating that a high vs. low S100 concentration is indicative of a more severe brain damage and injury, our results suggest that 90 s of only ventilation is too long without chest compressions to push blood out so that oxygenated blood can circulate to organs (including the brain) and peripheral tissue.…”

“…The choice of brain inflammation markers is somewhat limited but includes cytokines that rise within few hours after an inflammatory event (TNF-α and IL-6) (7-10); S100 (11,12), indicative of poor neurological outcome; ICAM-1 (15-17); the apoptosis pathway gene (caspase 3) (14); and MMPs (13,14), known to rise in pigs after hypoxia and reoxygenation. In group 3 (90 s), the CSF markers S100, IL-6, and TNF-α were elevated as compared with the reference group, and in the hippocampus tissue, MMP-9 and ICAM-1 genes appeared significantly differently expressed.…”

“…Alternatives to today's ventilation and chest compression guidelines may be easier to perform and teach and should be considered if the brain inflammatory response is of similar intensity. We chose to study a spectrum of inflammation markers in cerebrospinal fluid (CSF) and brain tissue by quantification of cytokines, interleukin-6 (IL-6) (7-9) and tumor necrosis factor-α (TNF-α) (10) and S100 (11,12) in CSF, and gene expression of matrix metalloproteinases (MMPs) (13,14), intercellular adhesion molecule 1 (ICAM-1) (15)(16)(17), the apoptosis-related cysteine peptidase caspase 3 (14), and cytokines IL-6 and TNF-α in the hippocampus and frontal cortex tissue. On the basis of our previous papers on return of spontaneous circulation (ROSC) (18)(19)(20)(21), we aimed to find out if initial ventilation periods longer than 30 s, compression-to-ventilation (C:V) ratios other than the 3:1, or air instead of pure oxygen may induce less brain injury and inflammation in extremely sick pigs.…”

S100B protein in serum is elevated after global cerebral ischemic injury

“…S100B protein in the serum of patients with traumatic brain injury (TBI) will rise rapidly within 6 hours after injury. Studies[9,10] have proved that the higher level of S100B protein in serum, the more risks the patients with TBI. It is also reported that S100B protein could predict the prognosis of patients with TBI.…”